Coordinatore | UNIVERSITAT WIEN
Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie. |
Nazionalità Coordinatore | Austria [AT] |
Totale costo | 1˙163˙832 € |
EC contributo | 1˙163˙832 € |
Programma | FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013) |
Code Call | ERC-2010-StG_20091118 |
Funding Scheme | ERC-SG |
Anno di inizio | 2011 |
Periodo (anno-mese-giorno) | 2011-03-01 - 2016-02-29 |
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1 |
UNIVERSITAT WIEN
Organization address
address: UNIVERSITATSRING 1 contact info |
AT (WIEN) | hostInstitution | 1˙163˙832.00 |
2 |
UNIVERSITAT WIEN
Organization address
address: UNIVERSITATSRING 1 contact info |
AT (WIEN) | hostInstitution | 1˙163˙832.00 |
Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.
'During autophagy initially small double membrane-bound structures expand and adopt cup-like shapes. These cup-shaped structures fuse at their rims to give rise to autophagosomes within which cytoplasmic material is enclosed. Subsequently autophagosomes fuse with endosomes and lysosomes and the content and the inner membrane are degraded. Autophagy serves to recycle essential building blocks during starvation, to degrade damaged organelles, to clear cells of protein aggregates and to kill intracellular microorganisms. Little is known about the mechanisms by which cells bend and remodel membranes into autophagosomes. The action of a complex containing type III PI3K activity is essential for the initiation of autophagosome formation. During expansion of the initial double membrane bound structure the Atg8 and Atg12 conjugation systems play important roles. A further protein that is essential for autophagosome formation is the transmembrane protein Atg9. We will investigate the impact of individual PI3K complex subunits, the Atg8 and Atg12 conjugation systems and Atg9 on membrane morphology in vitro. We will analyse membrane shape changes and micro-domain formation using artificial small and giant liposomes by electron and light microscopy. We will introduce targeted mutations that are designed to interfere with membrane shape changes or micro-domain formation. Furthermore, where necessary, we will solve the structure of individual subunits or complexes by x-ray crystallography. We will further verify our in vitro findings in cell culture systems. Our results will give important insights into autophagy and organelle formation in general.'